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. 2018 Dec 28;6(1):5.
doi: 10.3390/medicines6010005.

Chicken Protein Hydrolysates Have Anti-Inflammatory Effects on High-Fat Diet Induced Obesity in Mice

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Free PMC article

Chicken Protein Hydrolysates Have Anti-Inflammatory Effects on High-Fat Diet Induced Obesity in Mice

Thomas A Aloysius et al. Medicines (Basel). .
Free PMC article

Abstract

Background: Studies have shown that dietary source of protein and peptides can affect energy metabolism and influence obesity-associated diseases. This study aimed to investigate the impact of different chicken protein hydrolysates (CPHs) generated from chicken rest raw materials in a mouse obesity model. Methods: Male C57BL/6 mice were fed a high-fat, high-sucrose diet with casein or CPHs generated using Papain + Bromelain, Alcalase, Corolase PP, or Protamex for 12 weeks (n = 12). Body weight, feed intake, and intraperitoneal glucose tolerance was determined, and plasma and liver and adipose tissues were collected at sacrifice. Results: The average feed intake and body weight did not differ between the groups and white adipose tissue depots were unchanged, except for a reduction in the subcutaneous depot in mice fed the Protamex CPH diet. Moreover, the CPH diets did not prevent increased fasting glucose and insulin levels. Interestingly, the hepatic mitochondrial fatty acid β-oxidation was increased in mice fed Alcalase and Corolase PP CPHs. All CPH diets reduced plasma interleukine (IL)-1β, interferon-γ, tumor necrosis factor α, and monocyte chemotactic protein 1 compared to control, indicating anti-inflammatory effects. In addition, Corolase PP and Protamex CPHs significantly reduced plasma levels of IL-1α, IL-2, IL-6, IL-10, and granulocyte macrophage colony-stimulating factor. Conclusions: CPH diets were not able to counteract obesity and glucose intolerance in a mouse obesity model, but strongly reduced inflammatory parameters associated with obesity. Alcalase and Corolase PP CPHs also stimulated mitochondrial fatty acid β-oxidation. The possibility that hydrolysates from chicken rest raw materials could alleviate obesity-associated metabolic disease should be investigated further.

Keywords: chicken protein hydrolysate; cytokines; inflammation; liver; mitochondrial fatty acid oxidation; obesity; peptides; plasma lipids.

Conflict of interest statement

Norilia AS supported this study and is a commercial producer of the study material. They did not contribute to the choice of research project; design of the study; in the collection, analysis or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
Body weight and feed intake in C57BL/6 mice fed 19 E% casein- or 9.5 E% casein and 9.5 E% CPH-high fat/high sucrose diets for 12 weeks. (A) Body weight per mouse measured before and after week 1, 6, and 11, and at day of sacrifice. Mean values are shown (n = 12). (B) Total weight gain per mouse during the study. Mean values with standard deviations are shown (n = 12). (C) Feed intake per week per mouse measured during week 1, 6, and 11 of the study. Mean values were based on average feed intake per mouse per cage (n = 3). Significant difference between values were determined by one-way ANOVA with Fisher’s LSD test (* p < 0.05).
Figure 2
Figure 2
Weight percentage of body weight of white adipose tissue (WAT) depots in C57BL/6 mice fed 19 E% casein- or 9.5 E% casein and 9.5 E% CPH-high fat/high sucrose diets for 12 weeks. (A) The subcutaneous WAT depot on the right side of the body from fore- to hindlimb × 2. (B) The right side epididymal/gonadal WAT depot × 2. (C) The mesenteric WAT surrounding the intestines. (D) The right-side WAT depot surrounding and behind the kidney × 2. (E) The ratio between the weight percentage of body weight of visceral and subcutaneous WAT depots. Mean values with standard deviation are shown (n = 11–12). Significant difference between values were determined by one-way ANOVA with Fisher’s LSD test (* p < 0.05).
Figure 3
Figure 3
Fasting glucose and insulin levels in C57BL/6 mice at baseline (0 weeks) and after 11 weeks of feeding with 19 E% casein- or 9.5 E% casein and 9.5 E% CPH-high fat/high-sucrose diets. (A) The fasting blood glucose level. (B) The fasting plasma insulin level. (C) The fasting glucose and insulin ratio. Mean values with standard deviation are shown (n = 5–6). Significant difference between group mean values at 0 and 11 weeks was determined by one-way ANOVA with Fisher’s LSD test (all p > 0.05). Significant difference between mean values at 0 and 11 weeks within each group was determined by two-way ANOVA and Sidak’s multiple comparisons test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Figure 4
Figure 4
Intraperitoneal glucose tolerance (IP-GTT) in C57BL/6 mice at baseline (A) and after 11 weeks of feeding with 19 E% casein- or 9.5 E% casein and 9.5 E% CPH-high fat/high-sucrose diets (B). The increase in the area under the curve (AUC) from baseline to 11 weeks of feeding (C). Values are means with standard deviation (n = 5–6). Significant difference between values were determined by one-way ANOVA with Fisher’s LSD test (p < 0.05).
Figure 5
Figure 5
Hepatic β-oxidation in C57BL/6 mice fed high fat/high sucrose diets with casein (19 E%) or casein (9.5 E%) combined with different CPHs (9.5 E%) for 12 weeks. (A) In vitro β-oxidation of palmitoyl-CoA in fresh liver homogenates. (B) In vitro activity of acyl-CoA oxidase 1 (ACOX1) in frozen liver homogenates. Mean values with standard deviation are shown (n = 5–6). (C) Hepatic gene expression of carnitine palmitoyl transferase 1a (Cpt1a), Cpt2, hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit beta (Hadhb), and 2,4-dienoyl-CoA reductase 1 (Decr1). Mean values with standard deviation are shown (n = 7). Significant differences between values were determined by one-way ANOVA with Fisher’s LSD test (* p < 0.05).
Figure 6
Figure 6
Plasma and liver lipid levels in C57BL/6 mice fed 19 E% casein- or 9.5 E% casein and 9.5 E% CPH-high fat/high sucrose diets for 12 weeks (A) Plasma triacylglycerol (TAG), (B), plasma total cholesterol, (C) plasma phospholipids, (D) plasma non-esterified fatty acids (NEFA), (E) liver TAG, (F) liver cholesterol, (G) liver phospholipids, (H) liver NEFA. Values are means with standard deviation (n = 11–12). Significant differences between values were determined by one-way ANOVA with Fisher’s LSD test (* p < 0.05, ** p < 0.01, *** p < 0.001).
Figure 7
Figure 7
Plasma concentrations of (A) interleukin (IL)-1α, (B) IL-1β, (C) IL-2, (D) IL-6, (E) IL-10, (F) IL-17, (G) granulocyte colony-stimulating factor (G-CFS), (H) granulocyte macrophage colony-stimulating factor (GM-CFS), (I) interferon gamma (IFN-γ), (J) chemokine (C-C motif) ligand 5 (RANTES/CCL5), (K) tumor necrosis factor alpha (TNF-α), and (L) monocyte chemotactic protein 1 (MCP-1/CCL2),. Mean values with ranges are shown (n = 10–12). Significant differences between values were determined by one-way ANOVA with Fisher’s LSD test (* p < 0.05, ** p < 0.01, *** p < 0.001).

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